One of Candida albicans most impressive virulence attributes is the ability to propagate as a biofilm when attached to a medical device, such as a venous catheter. This critical factor alone is responsible for the majority of invasive and persistent disease. As conventional antimicrobials are ineffective for treatment of these life-threatening infections, further understanding of the biofilm lifestyle and how the cells survive drug therapy is desperately needed. The microbe-derived extracellular matrix, a distinguishing feature of biofilms, has been linked to several roles in biofilm pathogenesis. The proposed investigation capitalizes on our progress during the last funding period that identified the role o one matrix component, -1,3 glucan, for biofilm resistance and dispersion. Our excitement for future investigation is based upon two unexpected observations. First, we were surprised to find an abundance of two additional matrix polysaccharides, -1,6 glucan and -mannan. Second, we demonstrated an interaction among these matrix components. Our major objectives now are 1] to define the genetic pathways governing production, delivery, and maturation of the entire complement of polysaccharide matrix and 2] to discern how these matrix components function both individually and in a coordinated fashion during biofilm pathogenesis.